: 1) The LH receptor: The luteinizing hormone receptor (LHR) is an essential element in the control of gonadal cell function. Studies on the characterization of the human LHR gene has demonstrated the existence of genetic polymorphism with at least two forms of sequence heterogeneity within the exon-1 coding region spanning the junction of the signal peptide and the amino-terminus of the mature protein, which differ by the insertion of 6 bp. The more obvious difference between the two forms was the putative signal cleavage point. Both alleles are transcribed with prevalence of the allele without the insert in a random population, which may result from selection advantages with regard to the signal cleavage. Individuals homozygous for both forms displayed apparently normal reproduction. 2) The Prolactin receptor: Acting through its cognate receptor isoforms present in various target tissues, prolactin has a wide range of biological functions. The expression of the prolactin receptor (PRLR) is under the control of two tissue-specific promoters, PI (gonads) and PII (liver), and a common tissue promoter, PIII. Functional protein binding sites for C/EBPb and SP1/SP3 have been identified within the 258 bp promoter III . These widely expressed factors are the main activators of basal PIII activity. Also, an element down-stream from the main transcriptional start site is essential for basal promoter activity. The promoter III homolog in the mouse shares structural and functional similarities with that of the rat, whereas in the mouse the PI homolog is non-operative due to a mutation of the SF1 element. Taken together, these findings indicate that promoter III is of central importance in PRLR gene transcription across species, and the nature of the activators explains its common utilization in multiple tissues. Hormonal Control of Steroidogenesis: In the adult testis, gonadotropin (LH/hCG) exerts dual control of Leydig cell function. Low concentrations maintain LHR and steroidogenic enzymes and high concentrations cause down-regulation of LHR and desensitization of the steroidogenic pathway. Using in vivo and in vitro approaches and differential display analysis of Leydig cell mRNAs, we have demonstrated rapid hCG-induced negative regulation of type I and II mRNA transcription and protein expression of 3b-hydroxysteroid dehydrogenase (3b-HSD) in the Leydig cells of adult. This effect is independent of the down-regulation of the LH receptors. The consequent reduction in the activity of the enzyme could contribute to the inhibition of androgen production. In contrast, 3b-HSD mRNA transcripts were not changed in luteinized after upon high-dose gonadotropin treatment. The studies reflect gender specific regulation by the hormone to accomodate physiological hormonal requirements and reproductive function. .